diagnosis, classification and prevention
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Diagnosis, classification andprevention of diabetes
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Definition of diabetes
Characterized by hyperglycaemia
• Defects in insulin production
• Autoimmune or otherdestruction of beta cells
• Insulin insensiti ity• Impaired action of insulin on
target tissues
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Definition of diabetes
Chronic hyperglycaemia associated"ith long#term damage to$
• %yes
• &idneys
• 'er es• (eart and blood essels
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The diabetes epidemic
• 2!0 million affected in 200)
• !*0 million "ithin 20 years
• +ost rapid in Indian and Asiansubcontinents
ID, Diabetes Atlas
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World Statistics:
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Diagnosis and typesSlide ) of 48
Normal Pancreatic Islet:
ß cellsß cells (Insulin) αα cellscells (Glucagon)
δδ cellscells (Somatostatin) pp Cellspp Cells (pan prot)
ßß αα
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Diagnosis and typesSlide - of 48Insulin # Anabolic Steroid
• .ransmembrane transport of glucose
• /i er muscle 1 fat ↓ blood glucose
• /i er 1 s eletal muscle # ↑ glycogen
• Con erts glucose to triglycerides
• 'ucleic acid 1 3rotein synthesis
• DiabetesDiabetes Increased catabolism.Increased catabolism.• (yperglycemia ↓ protein synthesis /ipolysis
"asting "eight loss
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Cellular 6lucose pta e
Insulin "e#uiring
• Striated $uscle
• %ardiac $uscle
• &ibroblasts• & T
Non'Insulin "e#uiring
• 5lood 9essels
• 'er es
• &idney• %ye /ens
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Patholog( in Diabetes:
• )o* glucose inside cell ; decreased cell metabolism <muscle
li er=
• High glucose outside; 6lycosylation damage <59=; 3olyol products ; osmotic damage>
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%lassification
• .ype : diabetes
; autoimmune
; /ADA
; idiopathic
• .ype 2 diabetes
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?ther specific types
• +?D@
• Defects in insulin action• Diseases of the pancreas
• %ndocrine disorders
• Drug# or chemical#induced• Infections
%lassification
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• ncommon forms of immune#mediated diabetes
• ?ther genetic syndromes
• 6estational diabetes
%lassification
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Diagnosis and typesSlide :4 of 48
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Insulin
6luconeogenesis6lycogenolysis6lycogen synthesis
6lucose upta e6lycogensynthesis
5lood glucose
Insulin and glucose disposal
,ree fatty acid release
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Diagnosis and typesSlide :* of 48
T(pe + Diabetes
• 5eta cell destruction
• Absolute insulin deficiency
• sually immune#mediated
• Circulating mar ers of immune destruction<ICA IAA 6AD antibodies=
• arely obese at onset
• Associated "ith other autoimmune diseases<6ra eBs (ashimotoBs AddisonBs 3A itiligo=
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Diagnosis and typesSlide :) of 48
Pathogenesis of T(pe I D$GeneticGenetic
HLA-DR3/4HLA-DR3/4 EnvironmentEnvironmentViral infe..?Viral infe..?
Insulin deficiencInsulin deficienc! "e I / IDD#! "e I / IDD#
Autoimmune InsulitisAutoimmune InsulitisA$ to % cells/insulinA$ to % cells/insulin
ß cellß cellDestructionDestruction
• 3S 6lomerulonephritis• 6ra es (ashimoto thyroiditis• heumatic heart disease• S/% Collagen ascular disease• heumatoid arthritis
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6lucose upta e 6lycogenolysis 6luconeogenesis <amino acids= &etone production <fatty acids=
6lucose upta e 3rotein degradation → amino acids
5lood glucose
Insulin deficienc( int(pe + diabetes
.riglyceride degradation → fatty acids
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Diagnosis and typesSlide :7 of 48
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Pathogenesis of t(pe + diabetes
• Immunological acti ation
• 3rogressi e beta#cell destruction
• Insufficient beta#cell function
• Dependent on e ogenous insulin
• is of etoacidosis
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5eta#cellmass
Pathogenesis of t(pe + diabetes
.ime <months # years=
.rigger
6enetic
3re#diabetes (oneymoonB
%hronicphase
%linicaldiabetes
Immunologicalabnormalities
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Diagnosis and typesSlide 22 of 48
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Idiopathic t(pe + diabetes
'on#autoimmune type : diabetes
• 'o autoimmune mar ers
• 3ermanent insulinopenia
• &etoacidosis
• 3eople of African and Asian origin
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Diagnosis and typesSlide 2! of 48
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pidemiolog( of t(pe + diabetes
• Increasing in recent years
• 6eographic ariation
• elati e affluence
• /ac of treatment
ID, Diabetes Atlas
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• Age of onset pea s
; preschool; puberty
• AutumnE"inter pea s
pidemiolog( of t(pe + diabetes
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Diagnosis and typesSlide 2* of 48T(pe - Diabetes
• +ost ha e insulin resistance
• Insulin secretory defect
• elati e insulin deficiency
• 'o immune mar ers
• +ost are obese at onset
• &etosis may occur "ith stress
• 3rogressi e• 3art of Fdysmetabolic syndromeG
• Accounts for 70#7*H of ne" cases
i i d
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Diagnosis and typesSlide 2) of 48
T(pe - diabetes
• Characterized by chronic hyperglycemia
• Associated "ith micro ascular and macro ascularcomplications
• 6enerally arises from a combinationof insulin resistance andβ#cell dysfunction
Definition Diagnosis and Classification of Diabetes +ellitus and its Complications Department of 'oncommunicable Disease Sur eillanceorld (ealth ?rganization 6ene a :777 A ailable at$ http$EE""" diabetes org u EinfocentreEcarerecEdiagnosi doc
Di i d
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Diagnosis and typesSlide 2- of 48
IDD#IDD#
Genetic /Genetic / % cell defect% cell defect
Pathogenesis of T(pe II D$&$esit /&$esit /
Life st le ?Life st le ?
% cell% celle'(austione'(austion
! "e II )IDD#! "e II )IDD#
A$nor. *ecretionA$nor. *ecretionInsulin ResistanceInsulin Resistance
RelativeRelative
Insulin Def.Insulin Def.
Di i d
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Diagnosis and typesSlide 28 of 48
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6lucose upta e
6lycolysis
6luconeogenesis <amino acids=
6lucose upta e 3rotein degradation → amino acids
5lood glucose
Insulin insensitivit( in tt(pe - diabetes
Di i d t
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Diagnosis and typesSlide 27 of 48
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5lood glucose
6lucose upta e
Insensitivit( to insulin intt(pe - diabetes
6lucose upta e 6lycolysis
6luconeogenesis <amino acids=
6lucose upta e 3rotein degradation → amino acids
Di i d t
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5lood glucoseCon erted to triglycerides
ffect of insulin resistance in tt(pe - diabetes
6lucose upta e 6lycolysis
6luconeogenesis <amino acids=
6lucose upta e 3rotein degradation → amino acids
6lucose upta e
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Major defect in individuals with type 2diabetes 1
Reduced biological response to insulin 1–3
Strong predictor of type 2 diabetes 4
Closely associated with obesity
hat is insulin resistanceJ
I"
: American Diabetes Association Diabetes Care :778K 2:$!:0;!:425ec #'ielsen ( 1 6roop /C J Clin Invest :774K 74$:-:4;:-2: ! 5loomgarden L. Clin Ther :778K 20$2:);2!:
4(affner S+ et al. Circulation 2000K :0:$7-*;780 *5oden 6 Diabetes :77-K 4)$!;:0
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What is -cell dysfunction?
Major defect in individuals with type 2diabetes
Reduced ability of β!cells to secrete insulinin response to hyperglyce"ia
De,ronzo A et al. Diabetes Care :772K :*$!:8;
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Insulin resistance and -cell dysfunctionare core defects of type 2 diabetes
Insulinresistance
!eneticsusceptibilit(,
obesit(, Westernlifest(le
T(pe - diabetes
I" 'cell
d(sfunction
hodes CM 1 hite +, Eur J Clin Invest 2002K !2 <Suppl !=$!;:!
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#nsulin resistance – reduced response tocirculating insulin
Insulinresistance
!lucose output ↓ !lucose upta e ↓ !lucose upta e
H(pergl(cemia
)iver $uscle diposetissue
I"
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$hy does the β!cell fail%
%hronich(pergl(cemia
/versecretion ofinsulin tocompensate forinsulin resistance +,-
Highcirculatingfree fatt( acids
!lucoto0icit( -
Pancreas
)ipoto0icit( 1
'celld(sfunction
: 5oden 6 1 Shulman 6I Eur J Clin Invest 2002K !2$:4;2!2&aiser ' et al. J Pediatr Endocrinol Metab 200!K :)$*;22
! ,inegood D. 1 .opp 5 Diabetes Obes Metab 200:K ! <Suppl :=$S20;S2-
Diagnosis and types
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T(pe - diabetes
• 70H#7*H of people "ithdiabetes
• Insulin insensiti ity andrelati e insulin deficiency
• ?besity or o er"eight
• Complications often presentat diagnosis
Diagnosis and types
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Pathogenesis of t(pe - diabetes
• +ultiple genes in ol ed
• (yperinsulinaemia
• 3oor fetal nutrition → ↓ beta#cellformation
• /o" birth "eightE"eight change
• F.hrifty geneG
• -H beta#cell loss
Diagnosis and types
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Age <years=
%ndogenousinsulin
InsulinreNuirements
5eta#cell loss
The natural histor( oft(pe - diabetes
↑ Insulin
reNuirements"ith age
3rimaryfailure
Diagnosis and types
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Age <years=
%ndogenousinsulin
InsulinreNuirements
5eta#cell loss
Insulininsensiti ity
(yper#
insulinaemia
The natural histor( oft(pe - diabetes
↑ Insulin
reNuirements"ith age
Diagnosis and types
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Age <years=
%ndogenousinsulin
InsulinreNuirements
Secondaryfailure
The natural histor( oft(pe - diabetes
%ffect oforal drugs
↑ Insulin
reNuirements"ith age
5eta#cell loss
(yper#
insulinaemia
Insulininsensiti ity
Diagnosis and types
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pidemiolog( of t(pe - diabetes
• Dramatic increase
• Aging population
• Disturbing trends parallel obesityepidemic
• %specially in adolescents andminority groups
• Increasing in young people
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Type-I Type-II
&ess co""onChildren ' 2 (ears#nsulin! )ependent)uration* $ee+s
,cute Metabolicco"plications
,utoantibody* (es-a"ily .istory* /o#nsulin levels* very low#slets* #nsulitis
0 in twins
More co""on ,dult 2 (ears#nsulin #ndependent Months to years
Chronic ascularco"plications5/o(es/or"al or high /or"al 6 78haustion90!:0 in twins
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Insulitis – Type I
InsulinitisInsulinitis
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Islets in Type II Diabetes:
Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)
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Islets in Type II Diabetes:
Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)
Diagnosis and types
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"is factors for t(pe - diabetes
• Age O 40 years
• ,irst#degree relati e "ith diabetes
• +ember of high ris population
• (istory of impaired glucose toleranceimpaired fasting glucose
• 9ascular disease
• (istory of gestational diabetes
• (istory of deli ery of macrosomicbaby
CDA 200!
Diagnosis and types
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• (ypertension
• Dyslipidaemia
• Abdominal obesity• ? er"eight
• 3olycystic o ary disease
• Acanthosis nigricans
• Schizophrenia
"is factors for t(pe - diabetes
Diagnosis and types
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• 3olydipsia
• 3olyuria
• 'octuria
• 9isual disturbance
• ,atigue
• eight loss
• Infections
Signs and s(mptoms
Diagnosis and types
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Diagnosing diabetes
'ormal Impaired fasting glucose>
Impaired glucosetolerance>>
Diabetes
,36 P) :mmolE/
P::0mgEd/
) : to ) 7mmolE/>
::0 to :2)mgEd/
Q- 0mmolE/
Q:2)mgEd/
2hr 36 P- 8mmolE/
P:2)mgEd/
- 8 to ::mmolE/>>
:2) to 200mgEd/
Q:: :mmolE/
Q200mgEd/
CDA 200! ADA 2004 (? 2002
Diagnosis and types
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Impaired glucose toleranceImpaired fasting glucose
• Intermediate states
• Increased ris of de eloping diabetes• 3re ention strategies to pre ent or
delay progression
• Increased ris of cardio asculardisease
Diagnosis and types
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2ncertain diagnosis:/ral glucose tolerance test
• -* g glucose load after 8 hours
fasting
• eadings ta en in fasting stateand at : and 2 hours
• 3ossible problems
Diagnosis and types
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• rinary etones
• Antibodies
• C#peptide
Tests for differential diagnosis
Diagnosis and types
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$etabolic s(ndrome
• Cluster of ris factors or syndrome
• .ype 2 diabetes
• Different criteria
• .hree#fold increase in heartdisease and stro e
• ."o#fold increase in cardio asculardisease deaths
Diagnosis and types
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Prevention of t(pe + diabetes
• %arly e posure to co"s milprotein
• 'icotinamide
Diagnosis and typesl d f
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Prevention of t(pe + diabetes
Insulin
• Diabetes 3re ention .rial
• Diabetes 3rediction and3re ention 3roRect
Diagnosis and typesSlid *) f 48
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Prevention of t(pe - diabetes
/ifestyle modification
• Da ing Study
• ,innish Diabetes 3re ention Study
Diagnosis and typesSlid * f 48
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Prevention of t(pe - diabetes
/ifestyle s medication
• Diabetes 3re ention 3rogram
• S.?3#'IDD+
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Complications:
Short ter" Co"plications* ;"etabolic<.ypoglyce"ia)iabetic =etoacidosis/on =etotic hyperos"olar diabetic co"a&actic acidosis
&ong ter" Co"plications *;,ngiopathy<Microngiopathy ! Retinopathy>/ephropathy> /europhathy> der"atopathy5Macroangiopathy – ,therosclerosis5
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Microangiopathy athogenesis:
.yperglyce"ia chronic5?lycosylation of base"ent "e"braneproteins &ea+y blood vessels5
78cess deposition of proteins –glycosylation cycle5@hic+ and &ea+y blood vessels5/arrow lu"en#sche"ic Argan da"age555
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Diabetic Microangiopathy'ormal
Diabetic
6lucose6lycosylation5+ damage lea
A6%B deposition
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!europathy
Sensory Motor ;"yelin<Beripheral /europathy"ilateral# symmetric
rogressi$e# irre$ersible
araesthesia# pain# muscleatrophy
isceral neuropathyCranial ner$e – diplopia# "ell palsy
%IT- constipation# diarrhoeaC&' – orthostatic hypotension
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!europathy
+yelin loss in ner e
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Diabetic (myotrophy
3ainful muscle "asting
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Diabetic !europathic ulcer
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!europathic ulcer
%tiology$peripheral sensory
neuropathy .rauma1 deformity,actors$
Ischemia callusformation andedema
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!europathic ulcers
FEATURES:
Painless, surrounded by callusAt pressure points.associated with good foot pulsesMay not be associated with gangrene
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!ephropathy
/odular ?lo"eruloSclerosis5Co""on "orbidity "ortality5
)eposition of D,?7E ,dvanced ?lycosylation7nd!products as nodules5/ephrotic syndro"eByelonephritis7nd stage renal failure
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)iabetic /ephropathy
Microangiopathy> atherosclerosis infections*)iffuse or nodular diabeticglo"erulosclerosis ;=i""elstiel $ilson Sy<Renal arteriolosclerosis atherosclerosis/ecrotiFing renal papillitis5Byelonephritis57nd stage +idney5
!odular %lomerulosclerosis
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!odular %lomerulosclerosis –)W lesion*
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Diabetic %lomerulosclerosis
Hyaline nodulesHyaline nodules
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Diabetic %lomerulosclerosis
l
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!ormal +etina
l f $ h
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!on roliferati$e +etinopathyenous dilation and s"all red dots posterior retinal
pole ! capillary "icro!aneurys"s5Dot and blot retinal he"orrhages and deep!lyingede"a and lipid e8udates i"pair "acular function5&ate generaliFed di"inution of vision due toischemia and macular edema ! co""on cause ofvisual defect ;best detected by fluoresceinangiography<Cotton-,ool spots ;soft e8udates< ! "icroinfarctsdue to ische"ia5 @hey are white and obscureunderlying vessels5 .ard e8udates are caused bychronic ede"a5 @hey are yellow and generally deepto retinal vessels5
lif i$ i h
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roliferati$e +etinopathy/eovasculariFation ! which grows into the vitreouscavity5#n advanced disease> neovascular "e"branes canoccur> resulting in a traction retinal detach"ent5
itreous he"orrhages "ay result5sudden severe loss of vision can occur when there isintravitreal he"orrhage5Boor visual prognosis if severe retinal ische"ia>e8tensive neovasculariFation> or e8tensive fibroustissue for"ation5Banretinal photocoagulation "ay di"inish oreli"inate proliferative retinopathy
i h
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+etinopathy
/on BroliferativeMicroaneurys"s>)ot blot he"orrhages.ard and soft e8udates
Cotton wool – infarctsMacular ede"a5
Broliferative5/eovasculariFation&arge he"orrhagesRetinal detach"ent5
Di b i i h
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Diabetic +etinopathy
eo!ascularization Cotton "ool
spots
Di b i i h
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Diabetic +etinopathy
Dot blot ; (emorrhages <+icroaneurysms=
Di b i i h
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Diabetic +etinopathy
3re retinal (emorrhage # detachment
Di b ti + ti th
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Diabetic +etinopathy
Ad anced fibrous plaNues
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The past cannot be changed# but thefuture can** by actions in the present
time*. !!G=
ast is history#ast is history#
/uture is mystery/uture is mysteryresent is the gift01resent is the gift01
b l th di *
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abel the diagram*15253545
5
(ard dep?ptic disc+acula5lot hem
Cotton "ool
M i h h l i
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Macroangiopathy ,therosclerosis
)yslipide"ia↓ .)&
/on!7nFy"atic ?lycosylation
↑ Blatelet ,dhesiveness
↑ @hro"bo8ane , 2
↓ Brostacyclin
3ndothelial damage (therosclerosis
M#> C ,> ?angrene of &eg ;B )<> Renal
#nsufficiency
(th l i
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(therosclerosis:
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'lide 'ho,
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/ g l i f ti C didi i
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/ungal infections: Candidiasis
Macrosomia
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Macrosomia
ith 3olycythemia
"lood $essel calcification:
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lood $essel calcification:
Amputated thumb
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(canthosis !igricans
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(canthosis !igricans
Insulin resistanceT
(canthosis !igricans
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(canthosis !igricans
Insulin resistanceT
abel the diagram*
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abel the diagram*15253545
Capillary'odule ; A6%5o"man caps(yaline
arteriolosclerosis inarteriole
Infections in Diabetes:
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Infections in Diabetes:
)ecreased "etabolis" – low i""unity5)ecreased function of ly"phocytes neutrophils – glycosylation5?lycosylation of i""une "ediators5 ,bCapillary thic+ening – i"paired infla""ation5#sche"ia infarctions5
#ncreased glucose ;alone is not the cause <
)iabetes State of i""unosuppression5
aboratory Diagnosis:
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aboratory Diagnosis:
Hrine glucose ! dip!stic+ –ScreeningRando" or fasting blood glucose ;'11<-asting I""ol> Rando" 11""ol
#f -asting level is between I!11 then A?@@
.b,1c ! for follow!up> not for diagnosis
-ructosa"ine ! for long ter" "aintenance5
oints to remember:
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oints to remember:
)isorder of "etabolis" – #nsulin@ype!# Children> ,cute> Metabolic co"pl5@ype!## ,dults> Chronic> ascular co"pl5
,ngiopathy ;"icro6"acro<>.eart> Grain> =idney> Retina> S+in> G 5
#ncreased #nfections – +now reasons5
.ypoglyce"ia is "ore dangerous5 /ot hyper ?lucose control is critical -GS> ?@@ .b,1C5
4uestions**
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4uestions
.ow – =etoacidosis%.ow – hypoglyce"ia % ,ngiopathy – Macro Micro %
#nfections in@ypes of retinopathy %)iabetes insipidus %
/ephrotic 6 /ephritic syndro"e %=idney da"age in )iabetes %
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It5s not that I5m so smart#it5s 6ust that I stay ,ith
problems longer.!!,lbert 7instein
Diagnosis and typesSlide :02 of 48%TI3IT4
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.ype 2 diabetes can be delayed inpeople "ith I6.
/ifestyle modification is most
effecti e
hat do you thin could be done atcommunity le el to pre ent or delaydiabetesJ
Diagnosis and typesSlide :0! of 48
S mmar(
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Summar(
.ype : diabetes
• esults from progressi e beta#
cell destruction• 3eople "ith type : diabetes need
insulin therapy to li e
Diagnosis and typesSlide :04 of 48
Summar(
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.ype 2 diabetes
• ?ften characterized by insulin
insensiti ity and relati e ratherthan absolute insulin deficiency
• A progressi e condition
• +ost people "ith type 2 diabetes"ill need insulin "ithin * to :0years of diagnosis
Summar(
Diagnosis and typesSlide :0* of 48
"evie* #uestion
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evie* #uestion
: .he pathogenesis for type 2 diabetesincludes$
a Insulin deficiency and insulininsensiti ityb Insensiti ity to insulin and
autoimmune beta#cell destruction
c Autoimmune beta#cell destructionand glucagon deficiencyd Insulin deficiency and glucagon
deficiency
Diagnosis and typesSlide :0) of 48
"evie* #uestion
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evie* #uestion
2 A person "ith type 2 diabetes recentlystarted on insulin as s if there is a "ayto measure if heEshe is still producing any
insulin .he correct response "ould be$
a Islet cell antibody tests
b C#peptide test
c (bA :c test
d Serum insulin test
Diagnosis and typesSlide :0- of 48
"evie* #uestion
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evie* #uestion
! .he Diabetes 3re ention 3rogram <D33=$
a Included people "ith type :
diabetesb Included only people "ith I6.
c .ested the alue of e ercise
d Included people "ith type 2diabetes
Diagnosis and typesSlide :08 of 48
"evie* #uestion
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evie* #uestion
4 .ype : diabetes is usually caused by$
a InRury to the pancreas
b An autoimmune reaction
c Insulin insensiti ity in the cells
d (ypersensiti ity to insulin
Diagnosis and typesSlide :07 of 48
ns*ers
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ns*ers
: a
2 b
! b
4 b
Diagnosis and typesSlide ::0 of 48
"eferences
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Slides current until 2008
eferences
: American Diabetes Association Diagnosis and classification of diabetes mellitus Diabetes Care
2004K 2-<suppl :=$ S*#S:02 Canadian Diabetes Association Clinical 3ractice 6uidelines % pert Committee Canadian
Diabetes Association 200! clinical practice guidelines for the pre ention and management ofdiabetes in Canada Can M Diab 200!K 2-<suppl 2=
! Chiasson M/ Mosse 6 6omis et al Acarbose for pre ention of type 2 diabetes mellitus$.he S.?3#'IDD+ randomized trial /ancet 2002K !4)$ !7!#40!
4 Delahanty /+ and (alford 5' .he role of Diet 5eha iours in Achie ing impro ed glycaemic
control in intensi ely treated patients in the Diabetes Control and Complications .rial DiabetesCare :77!K :)<::=$ :4*!#*8
* Diabetes Control and Complications .rial esearch 6roup %ffect of intensi e diabetestreatment on the de elopment and progression of long#term complications in adolescents "ithinsulin dependent diabetes mellitus$ Diabetes Control and Complications .rial .he Mournal of3aediatrics :774K :2*<2=$ :--#88
) Diabetes Control and Complications .rialEepidemiology of diabetes inter entions andcomplications research group intensi e diabetes therapy and carotid intima#media thic ness intype : diabetes mellitus 'e" %ngl M +ed 200!K !48$ 2274#!0!
- Diabetes Control and Complications .rial$ .he effect of intensi e treatment of diabetes on thede elopment and progression of long#term complications in insulin#dependent diabetesmellitus ' %ngl M +ed :77!K !27$ 7--#8)
Diagnosis and typesSlide ::: of 48
"eferences
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Slides current until 2008
eferences
8 ,ord %S 6iles ( Dietz ( 3re alence of the metabolic syndrome among S adults$ findingsfrom the third 'ational (ealth and 'utrition % amination Sur ey MA+A 2002K 27-$ !*)#*7
7 Diabetes Atlas 200) 5russels$ International Diabetes ,ederation 200)
:0 Isomaa 5 Almgren 3 .uomi . et al Cardio ascular morbidity and mortality associated "ith themetabolic syndrome Diabetes Care 200:K 24<4=$ )8!#7
:: 3an U /i 6 (u @ et al %ffects of diet and e ercise in pre enting 'IDD+ in people "ith impairedglucose tolerance$ .he Da ing I6. and Diabetes Study Diabetes Care :77-K 20<4=$ *!-#44
:2 eport of a (? Consultation /aboratory Diagnosis and monitoring of Diabetes +ellitus orld
(ealth ?rganisation 2002 http$EE"hNlibdoc "ho intEhNE2002E724:*7048! pdf cited April !0200*
:! .uomilehto M /indstrom M %ri sson M6 et al 3re ention of type 2 diabetes mellitus by changes inlifestyle among subRects "ith impaired glucose tolerance ' %ng M +ed 200:K !44$ :!4!#*0
:4 .he Diabetes 3re ention 3rogram esearch 6roup .he diabetes pre ention 3rogram <D33=Diabetes Care 2002K 2!<:2=$ 2:)*#-:
:* & 3rospecti e Diabetes Study 6roup Intensi e blood#glucose control "ith sulpfonylureas or
insulin compared "ith con entional treatment and ris of complications in patients "ith type 2diabetes /ancet :778K !*2$ 8!-#*!
Diagnosis and typesSlide ::2 of 48
"eferences
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eferences
:) & 3rospecti e Diabetes Study 6roup .ight blood pressure control and ris ofmacro ascular and micro ascular complications in type 2 diabetes &3DS !8 5+M
:778K !:-$ -0!#:!
:- ID, Clinical 6uidelines .as ,orce 6lobal 6uideline for .ype 2 Diabetes 5russels$International Diabetes ,ederation 200*
:8 (arris S5 % oe M+ Ldano"icz @ ebster#5ogaert S 6lycemic Control andmorbidity in the Canadian primary care setting <results of the diabetes in Canadae aluation study= Diab esearch and Clin 3ract 200*K -0$ 70#-